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Nursing Pharmacology > Module 13 - Part 2 > Flashcards

Module 13 - Part 2 Flashcards

1
Q

______ are the mainstay of therapy for HTN.

A

diuretics

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2
Q

What are the three main classes of diuretics?

A

Loop diuretics
Thiazide diuretics
potassium sparing diuretics/aldosterone antagonists

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3
Q

Diuretics work by blocking ______ and ________ ion reabsorption from the nephron of the kidney.

A

sodium

chloride

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4
Q

By preventing the reabsorption of Na+ and Cl-, diuretics make an osmotic pressure within the tubule that prevents the _____ of _______.

A

reabsorption of water

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5
Q

Diuretics produce more _______ decreases in BP at sites of ____ sodium reabsorption.

A

effective

high

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6
Q

______ diuretics produce the largest decrease in BP since 20% of sodium is reabsorbed at its site of action.

A

Loop diuretics (the most effective diuretics available

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7
Q

Mechanism of action of loop diuretics?

A

They act by blocking sodium and chloride ion reabsorption in the thick ascending limb of the LoH

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8
Q

Loop diuretics are usually reserved for situations that required rapid loss of fluid such as? (3)

A

Edema
Severe HTN that does not respond to milder diuretics
Severe renal failure

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9
Q

What are the adverse effects of Loop diuretics?

A

Hypokalemia
Hyponatremia
Dehydration
Hypotension

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10
Q

Low potassium levels in the blood, may also cause fatal ______ ________.

A

Hypokalemia

may cause fatal cardiac dysrhythmias

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11
Q

Why does hypokalemia occur as an adverse effect when taking loop diuretics if they decrease sodium reabsorption?

A

The transporter responsible for reabsorbing Na+ and Cl- also transports K+ into the blood, which is why hypokalemia occurs

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12
Q

Most commonly used class of drugs to treat HTN

A

Thiazide diuretics

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13
Q

Thiazide diuretics act by two main mechanisms, what are these?

A

Blocking sodium chloride ion reabsoprtion in the distal tubule
Decreasing vascular resistance (unknown mechanism)

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14
Q

For many hypertensive patients, thiazide diuretics alone _____ enough to control BP.

A

are

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15
Q

Adverse effects of thiazide diuretics?

A

Hypokalemia - may cause fatal cardiac dysrhythmias
Dehydration
Hyponatremia

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16
Q

Potassium sparring diuretics are also called this.

A

Aldosterone antagonists

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17
Q

Aldosterone Antagonists/Potassium sparing diuretics mechanism of action?

A

Act by inhibiting aldosterone receptors in the collecting duct
Blocking these receptors causes increased sodium excretion and potassium retention

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18
Q

What is the main use of potassium sparing diuretics?

A

Main use is in combination with thiazide and loop diuretics to counteract hypokalemia side effect

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19
Q

Potassium sparring diuretics should not be used with these.

A

Ace inhibitors or renin in inhibitors

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20
Q

What is the primary side effect of potassium sparring diuretics?

A

Hyperkalemia - may result in fatal dysrhythmias

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21
Q

Beta blockers are effective at treating HTN and they do this through two distinct mechanisms, what are these?

A

Blocking cardiac beta 1 receptors

Blocking beta 1 receptors on juxtaglomerular cells

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22
Q

What does blocking beta 1 receptors do?

A

Blocks catecholamine (e.g. epinephrine) binding to beta 1 receptors, decreasing CO and thus BP

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23
Q

What does blocking beta 1 receptors on juxtaglomerular cells do?

A

Beta blockers decrease renin release and therefore decrease RAAS mediated vasoconstriction

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24
Q

Beta blockers all have this suffix.

A

“olol”

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25
Q

What are the beta blocker classes?

A

1st generation (non-selective) and 2nd generation beta blockers (selective)

26
Q

Inhibit both beta 1 (heart and juxtaglomerular cells) and beta 2 (lung) receptors

A

1st generation beta blockers

27
Q

1st generation beta blocker use can be problematic in what instances?

A

If patients have asthma or other lung disorders

28
Q

Produce selective blockage of beta 1 receptors

A

2nd generation beta blockers

29
Q

What are the adverse effects of 2nd generation beta blockers?

A

Bradycardia, decreased CO, heart failure rare, rebound hypertension/cardiac excitation is withdrawn abruptly

30
Q

How can rebound hypertension/cardiac excitation be avoided?

A

By tapering the dose of beta blockers slowly over 10-14 days

31
Q

What additional adverse effects do non-selective beta blockers have?

A

Bronchoconstriction

inhibition of hepatic and muscle glycogenolysis

32
Q

The inhibition of hepatic and muscle glycogenolysis can be dangerous to which types of patients?

A

Patients with diabetes if they accidentally take too much insulin

33
Q

How do ACE inhibitors decrease BP?

A

Decrease angiotensin II production

Inhibit the breakdown of bradykinin

34
Q

Decreased angiotensin II causes what?

A

Decreased PVR and total blood volume, thus CO

35
Q

Inhibiting the breakdown of bradykinin has what effect?

A

Elevated bradykinin leads to vasodilation

36
Q

ACE inhibitors have this suffix.

A

“ipril”

37
Q

What are the ACE inhibitor side effects related to decreased angiotensin II?

A

1st dose hypotension

Hyperkalemia

38
Q

Due to 1st dose hypotension with ACEI’s, what is done?

A

first few doses should be low

39
Q

Why is hyperkalemia a side effect of ACE inhibitor use?

A

Decreased angiotensin II means decreased aldosterone release, thus decreased sodium reabsorption and thus greater potassium reasborption – should avoid use with potassium sparing diuretics

40
Q

What are the side effects related to increased bradykinin?

A

Persistent cough

Angioedema

41
Q

Use of certain _______ may decrease the effects of ACE inhibitors.

A

NSAIDs

42
Q

Similar action to ACE inhibitors, but the mechanism differs.

A

Angiotensin receptor blockers (ARBs)

43
Q

Mechanism of action of ARBs.

A

Block the binding of angiotensin II to the AT1 receptor (do not block its synthesis), this causes vasodilation and decreased aldosterone release from the adrenal cortex

44
Q

ARBs have this suffix.

A

“sartan”

45
Q

What are the side effects of ARBs?

A

Although we would expect the sides to match up with ACE inhibitors, there is no hyperkalemia, or persistent cough, and the incidence of angioedema is much lower

46
Q

What is the mechanism of action of direct renin inhibitors?

A

Bind to renin and block the conversion of angiotensinogen to angiotensin I
This is the rate limiting step of the RAAS pathway, and thus the entire pathway is affected.

47
Q

What are the adverse effects associated with DRIs?

A

Hyperkalemia
Very low incidence of persistent cough and angioedema
Diarrhea

48
Q

DRIs should never be used with these.

A

Potassium sparing diuretics

49
Q

How do calcium channel blockers decrease BP?

A

Block the entry of calcium into the heart cells and smooth muscle cells, therefore decreasing contraction

50
Q

What are the two categories of calcium channel blockers?

A

Dihydropyridine calcium channel blockers

Non-dihydropyridine calcium channel blockers

51
Q

At therapdeutic doses, dihydropyridine calcium channel blockers do not affect this.

A

The heart - effect exclusive to smooth muscle around arteries

52
Q

What is the suffix of dihydropyridine calcium channel blockers?

A

“dipine”

53
Q

What are adverse effects of dihydropyridine calcium channel blockers?

A

flushing, dizziness, headache, peripheral edema, reflex tachycardia, rash

54
Q

What is the difference between dihydropyridine calcium channel blockers and non-dihydropyridine calcium channel blockers?

A

The non-hydridopyrimidine counterparts also block calcium channels in the heart and thus also decrease CO.

55
Q

What are the adverse effects of non-dihydropyridine calcium channel blockers?

A

constipation, dizziness, flushing, headache, edema, may compromise cardiac function and should be used with caution in patients with cardiac failure

56
Q

What is the mechanism of action of centrally acting alpha 2 agonists?

A

bind to and activate alpha 2 receptors in the brainstem –> activation of these receptors decreases sympathetic outflow to the heart and blood vessels, thereby decreasing CO and peripheral resistance

57
Q

What are adverse effects of centrally acting alpha 2 agonists?

A

drowsiness, dry mouth, rebound HTN if withdrawn abruptly

58
Q

The target BP that most patients should achieve is less than this.

A

140/90 torr

59
Q

Patients with diabetes or chronic kidney disease should achieve a blood pressure less than this.

A

130/80 torr

60
Q

In patients with severe renal disease, ______ diuretics are ineffective so _____ diuretics should be used.

A

thiazide

loop

Nursing Pharmacology (30 decks)

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